Congestive heart failure (CHF) is a debilitating, end-stage disease in which abnormal function of the heart leads to inadequate blood flow to fulfill the needs of the body's tissues. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately fill with blood between heartbeats and the valves regulating blood flow may become leaky, allowing regurgitation or back flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness, and inability to carry out daily tasks may result.
Not all CHF patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive.
As CHF progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output.
CHF has been classified by the New York Heart Association (NYHA). Their classification of CHF corresponds to four stages of progressively worsening symptoms and exercise capacity from Class I to Class IV. Class I corresponds to no limitation wherein ordinary physical activity does not cause undue fatigue, shortness of breath, or palpitation. Class II corresponds to slight limitation of physical activity wherein such patients are comfortable at rest, but where ordinary physical activity results in fatigue, shortness of breath, palpitations, or angina. Class III corresponds to a marked limitation of physical activity wherein, although patients are comfortable at rest, less than ordinary activity will lead to symptoms. Class IV corresponds to inability to carry on any physical activity without discomfort, wherein symptoms of CHF are present even at rest and where with any physical activity, increased discomfort is experienced.
Current standard treatment for heart failure is typically centered around medical treatment using ACE inhibitors, diuretics, and digitalis. It has also been demonstrated that aerobic exercise may improve exercise tolerance, improve quality of life, and decrease symptoms. Only an option in approximately 1 out of 200 cases, heart transplantation is also available. Other cardiac surgery is also indicated for only a small percentage of patients with particular etiologies. Although advances in pharmacological therapy have significantly improved the survival rate and quality of life of patients, patients in NYHA Classes III or IV, who are still refractory to drug therapy, have a poor prognosis and limited exercise tolerance. Cardiac pacing has been proposed as a new primary treatment for patients with drug-refractory CHF.
By tracking the progression or regression of CHF more closely, treatments could be administered more effectively. Commonly, patients adapt their lifestyle and activities to their physical condition. The activity level of the patients with NYHA Class III or IV would be much lower than that of the patients with NYHA Class I or II. The change in lifestyle or activity level, due to the patient's heart condition, will be reflected by activity and respiration physiological parameters.
Besides various assessments of the cardiac function itself, assessment of activity and respiration are typically performed. This includes maximal exercise testing in which the heart rate and maximum ventilation are measured during peak exertion. However, peak exercise performance has been found to not always correlate well with improvements in a patient's clinical conditions. Therefore, sub-maximal exercise testing can also be performed, such as a six-minute walk test. While improvements in sub-maximal exercise may suggest an improvement in clinical condition, sub-maximal exercise performance can be variable in that it is dependent on how the patient happens to be feeling on the particular day of the test.
As CHF progresses, the dilation of the heart chambers alters the normal conduction time of the electrical signals through the heart. These electrical signals coordinate the depolarization and subsequent contraction of the heart chambers. Bi-ventricular pacing is expected to improve the coordination of heart chambers by reducing the right ventricle (RV) contraction time and the left ventricle (LV) contraction time, and by increasing the diastolic filling time.
One challenge in bi-ventricular pacing is the ability to detect and verify capture of both ventricles. Since the benefit of bi-ventricular pacing is derived only when capture of both chambers is achieved, proper determination of pacing threshold for each ventricle, or both combined, is imperative to a successful therapy delivery. During device implantation, physicians often rely on ECG recordings to observe when a stimulating pulse is of sufficient energy to cause heart contraction, a condition known as “capture.” The lowest stimulation pulse energy sufficient to capture the heart is referred to as “capture threshold.”
FIGS. 3A, 3B and 3C depict three surface ECG recordings for three exemplary capture situations during bi-ventricular pacing. FIG. 3A represents a surface ECG recording during sub-threshold bi-ventricular pacing, and illustrates the failure to capture both the left and right ventricles. FIG. 3A shows a stimulation pulse 120 followed by a natural depolarization complex 124, with a time delay 125 therebetween. In FIG. 3A neither ventricle is captured, and the intrinsic responses of both ventricles are represented by the depolarization complex 124.
FIG. 3B represents a surface ECG during bi-ventricular pacing in which the capture of only one ventricle (i.e., the right ventricle) but not the other ventricle (i.e., the left ventricle) is achieved. A ventricular stimulation pulse 126 is followed immediately by a depolarization complex 127 which is a complex representing both the evoked response of the captured ventricle and the intrinsic response of the other ventricle that has not been captured. The evoked response to the stimulation pulse 126 in one ventricle is conducted naturally to the other ventricle causing a second depolarization. The conducted response of the other ventricle slightly lags the evoked response in the captured ventricle in accordance with the inter-ventricular conduction delay. This slight delay, however, is not distinguishable on the surface ECG. Since two distinct events are not easily discernible, recognition of only single-chamber capture versus bi-ventricular capture from the ECG recording alone is quite difficult.
FIG. 3C represents a surface ECG during bi-ventricular pacing when successful capture of both ventricles is achieved. A stimulation pulse 128 is followed immediately by a depolarization complex 129 representing the evoked response of both ventricles. This ECG recording appears generally similar to the ECG recording of FIG. 3B in which only one chamber was captured. As a result, differentiation between single-chamber capture (FIG. 3B) and bi-ventricular capture (FIG. 3C) is therefore difficult and impractical from a surface ECG recording. An inappropriately selected ventricular stimulation pulse energy could be harmful to the patient if only one ventricle is captured because poor synchronization between chambers could lead to arrhythmias.
Implantable cardiac stimulating devices contain sensing circuitry for monitoring the patient's internal heartbeat signals. These internal heartbeat signals are commonly referred to as the intracardiac electrogram (“IEGM”). Cardiac stimulating devices monitor the IEGM to determine precisely when stimulation pulses should be applied. For example, some implantable cardiac stimulating devices such as demand pacemakers apply electrical stimulation pulses to the heart only in the event that the patient's heart fails to beat properly on its own. By applying stimulation pulses only when needed, it is possible to avoid competition between the pulses applied by the device and the patient's intrinsic cardiac rhythm.
Cardiac stimulating devices process the IEGM to determine what type of electrical pulses should be applied to the patient's heart. Other cardiac devices, known as cardiac monitoring devices, are used solely to monitor the patient's cardiac condition. Cardiac monitoring devices are similar to cardiac stimulating devices, but do not contain pulse generating circuitry. Both cardiac stimulating devices and cardiac monitoring devices process the IEGM to identify various cardiac events. For example, an implantable cardiac device with atrial sensing circuitry can detect P-waves that accompany atrial contractions. Ventricular sensing circuitry can be used to detect R-waves that accompany the contraction of the patient's ventricles.
Cardiac stimulating devices additionally process the IEGM in order to verify that a stimulating pulse is of sufficient energy to capture. The lowest capture threshold is sought in order to conserve battery energy while maintaining effective therapy delivery. Numerous schemes for processing the IEGM to determine threshold and to detecting capture are described for example in U.S. Pat. No. 5,766,229 to Bornzin, U.S. Pat. No. 5,778,881 to Sun et al., and U.S. Pat. No. 5,324,310 to Greeninger et al.
However, conventional capture detection methods generally address the need to determine threshold and to verify capture in single-chamber pacing, specifically the right ventricle, or dual chamber pacing, specifically the right atrium and right or left ventricle. Therefore, a need still exists to detect threshold and capture during multi-chamber pacing configurations, particularly during bi-ventricular pacing in CHF patients.
In dual-chamber atrial-ventricular pacing, an atrial pulse generator and atrial sense amplifier are connected to the atrial lead, and a ventricular pulse generator and ventricular sense amplifier are connected to a ventricular lead. This allows separate sensing of atrial events and ventricular events to allow for distinct monitoring of atrial and ventricular threshold and capture detection. In a bi-ventricular pacing system, however, the ventricular channel can be bifurcated and connected to both the right ventricle lead and the left ventricle lead, with typically only one ventricular sense amplifier and one ventricular pulse generator, thus preventing the ventricles from being monitored or paced separately. Therefore, a method is needed that allows monitoring of the right ventricle and the left ventricle threshold and capture detection using existing hardware or circuitry.
Furthermore, a method of tracking the progression or regression of CHF during delivery of chronic pacing therapies would allow treatment to be administered more effectively.
A number of attempts have been made previously to provide for chronic monitoring of physiological parameters associated with CHF using implantable cardiac devices, such as pacemakers, in conjunction with physiological sensors. Reference is made to U.S. Pat. No. 5,518,001 to Snell et. al.; U.S. Pat. No. 5,944,745; U.S. Pat. No. 5,974,340 to Kadhiresan; U.S. Pat. No. 5,935,081 to Kadhiresan; U.S. Pat. No. 6,021,351 to Kadhiresan et al.
However, as CHF progresses, the dilation of the ventricles increases, causing inter-ventricular conduction time to increase. Therefore, it would be desirable to have a method that automatically and accurately monitors inter-ventricular conduction time during bi-ventricular pacing as a means for monitoring CHF progression.